QKI is an RNA-binding protein with multi-functional roles in post-transcriptional gene regulation. Primarily, it recognizes and binds mRNAs modified by internal N(7)-methylguanine (m7G) and interacts with G3BP1 to localize these transcripts into stress granules, suppressing their translation during stress 1. QKI also functions as a negative regulator of angiogenesis by binding mRNAs encoding CDH5, NLGN1, and TNFAIP6 to promote their degradation 2. Additionally, QKI stabilizes miR-122 by recruiting poly(A) polymerase TENT2 for 3' adenylation 3. Mechanistically, QKI acts as a splicing factor regulating circular RNA biogenesis. It promotes circBCAR3 formation by juxtaposing circularized exons in pre-mRNA 4, and similarly facilitates hsa_circ_0007919 splicing and circularization 5. QKI binds thousands of transcriptome-wide sites containing defined sequence motifs, showing preferences for specific transcript regions 6. Clinically, QKI dysregulation associates with cancer progression. In pancreatic cancer, elevated QKI promotes a basal-like, chemoresistant phenotype by repressing classical-subtype splicing events while promoting basal-like events associated with shorter survival 7. MYB/MYBL1::QKI fusions occur in gliomas, with additional mutations potentially driving malignant transformation 8. QKI participates in extracellular vesicle RNA packaging, influencing disease-relevant cell communication 9.